Un théologien "structuraliste" de l'ancienne Egypte

A Structuralist Theologian in Ancien Egypt This paper tries to prove that the 37th maxim of the Ani's teaching (XVIIIth dynasty) about the advisable attitude with respect to the god during his oracular processions, also contains a premature structuralist description of the deity and his material hypostasis ; this description squares with the binary vision of the Egyptian gods as proposed by Ph. Derchain.Dans la maxime 37 de son enseignement, le scribe égyptien Ani (nouvel empire) décrit la nature de la divinité et celle de la relation du dieu à ses effigies. En cela, il se révèle être un remarquable théologien, et son texte peut être interprété en l'intégrant à une structure semblable à celles que préconise Philippe Derchain. Le dieu se définit par rapport aux oppositions « réel-imaginaire », « visible-invisible », « proche- lointain » ; il se manifeste dans le réel proche et concret accessible à l' homme (statue) par la médiation de ses "baou" (« facultés d'accéder à l'autre face du monde »).Cannuyer Christian. Un théologien "structuraliste" de l'ancienne Egypte. In: Revue de l'histoire des religions, tome 202, n°2, 1985. pp. 147-160

DNA methylation and nucleosome occupancy regulate the cancer germline antigen gene MAGEA11

MAGEA11 is a cancer germline (CG) antigen and androgen receptor co-activator. Its expression in cancers other than prostate, and its mechanism of activation, has not been reported. In silico analyses reveal that MAGEA11 is frequently expressed in human cancers, is increased during tumor progression, and correlates with poor prognosis and survival. In prostate and epithelial ovarian cancers (EOC), MAGEA11 expression was associated with promoter and global DNA hypomethylation, and with activation of other CG genes. Pharmacological or genetic inhibition of DNA methyltransferases (DNMTs) and/or histone deacetylases (HDACs) activated MAGEA11 in a cell line specific manner. MAGEA11 promoter activity was directly repressed by DNA methylation, and partially depended on Sp1, as pharmacological or genetic targeting of Sp1 reduced MAGEA11 promoter activity and endogenous gene expression. Importantly, DNA methylation regulated nucleosome occupancy specifically at the -1 positioned nucleosome of MAGEA11. Methylation of a single Ets site near the transcriptional start site (TSS) correlated with -1 nucleosome occupancy and, by itself, strongly repressed MAGEA11 promoter activity. Thus, DNA methylation regulates nucleosome occupancy at MAGEA11, and this appears to function cooperatively with sequence-specific transcription factors to regulate gene expression. MAGEA11 regulation is highly instructive for understanding mechanisms regulating CG antigen genes in human cancer